1,358
Views
21
CrossRef citations to date
0
Altmetric
Autophagic Punctum

KIAA1524/CIP2A promotes cancer growth by coordinating the activities of MTORC1 and MYC

&
Pages 1352-1354 | Received 11 Apr 2014, Accepted 30 Apr 2014, Published online: 15 May 2014

Figures & data

Figure 1. Proposed model for the regulation of tumor growth by KIAA1524/CIP2A and autophagy. KIAA1524/CIP2A inhibits PP2A-mediated dephosphorylation of MTORC1 substrates RPS6KB1 and EIF4EBP1 thereby enhancing the MTORC1 signaling pathway. Together with previously reported effects of KIAA1524/CIP2A on stabilization of MYC, activation of E2F1 and AKT as well as inhibition of DAPK1, KIAA1524/CIP2A enhances tumor cell growth by stimulating protein synthesis, cell metabolism and proliferation as well as by inhibiting apoptosis. Conversely, MTORC1 inhibition leads to autophagic degradation of KIAA1524/CIP2A and reversal of its tumor-promoting activities.

Figure 1. Proposed model for the regulation of tumor growth by KIAA1524/CIP2A and autophagy. KIAA1524/CIP2A inhibits PP2A-mediated dephosphorylation of MTORC1 substrates RPS6KB1 and EIF4EBP1 thereby enhancing the MTORC1 signaling pathway. Together with previously reported effects of KIAA1524/CIP2A on stabilization of MYC, activation of E2F1 and AKT as well as inhibition of DAPK1, KIAA1524/CIP2A enhances tumor cell growth by stimulating protein synthesis, cell metabolism and proliferation as well as by inhibiting apoptosis. Conversely, MTORC1 inhibition leads to autophagic degradation of KIAA1524/CIP2A and reversal of its tumor-promoting activities.